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Introduction: Amiodarone as an antiarrhythmic medication is necessary in the prevention and treatment of malignant ventricular arrhythmias, however, it can induce thyroid dysfunction. Thyroid dysfunction may be either hypothyroidism or thyrotoxicosis, however, 50% of patients who have used amiodarone are euthyroid. Case report: A 27-year-old female patient, hospitalized at the Clinic for Endocrinology due to type 2 amiodarone-induced thyrotoxicosis. The patient had previously received amiodarone for two years. At age 25, the patient was diagnosed with dilated cardiomyopathy (EF 25%, EDD/ESD 56-57/47 mm) with mild Ebstein’s anomaly, WPW Sy and recorded episodes of non-sustained VT. In order to reduce the risk of sudden death and prevent malignant ventricular arrhythmias, ICD-VR was implanted and amiodarone was prescribed. Treatment with propylthiouracil (PTU) and dexamethasone was initiated after thyrotoxicosis was diagnosed. Three weeks after the introduction of PTU, hepatotoxicity was registered, thus the medication was discontinued. Thyrozol, which regulates the hepatotoxicity parameters, was introduced. Sodium perchlorate and glucocorticoid (per os, IV and intrathyroidal) therapy was introduced. The treatment had lasted for fifty days and laboratory signs of thyrotoxicosis were still present, which is why a total of eight plasmapheresis sessions were performed. Each plasmapheresis resulted in a significant decrease in FT4 and a slight decrease in FT3. After seventy two days of treatment, an optimal hormonal status of the thyroid gland was established and total thyroidectomy was performed. Conclusion: Patient was treated for amiodarone-induced thyrotoxicosis (AIT) type 2, which was resistant to conventional therapy for a long period of time. Successful treatment was achieved by applying plasmapheresis although the effect of perchlorate and glucocorticoids application cannot be disregarded.

The increased secretion of thyroid gland hormones affects the cardiovascular system by increasing heart rate and often by increasing systolic and diastolic blood pressure. We examined the influence of elevated thyroid hormone on blood pressure. Blood pressure monitoring was performed prior to the introduction of therapy in people with increased FT4 and on therapy when FT4 was in the normal range. We analyzed 32 people, of which 26 women had normal blood pressure values measured by blood pressure monitoring. Average age 45 and body mass index 27 kg/m2. Blood pressure was measured by monitoring blood pressure for 24 hours. On average, before the introduction of the therapy, it was 133/83 mmHg P 96 / min. The blood pressure on average on therapy with tireosuppressive was 128/82 mmHg P 74 / min. The Wilcoxon-Mann-Whitney paired test shows a significant P

Introduction: The most common cause for persistent elevation of TSH levels in hypothyroid patients treated with levothyroxine is poor compliance. The Levothyroxine Absorption Test (LAT) is usually confirmed this phenomenon called 'pseudo-malabsorption'. Case report: 60-year-old female, weight 60kg, BMI 24.3kg/m2, presented with sleepiness, tiredness, fatigue and forgetfulness. Her skin was very dry and flaky. She had low tolerance of effort, poor appetite with weight oscillation around 2kg, constipation and sometimes heartburn. Hypothyroid for ten years after radioiodine treatment of Graves' disease. Her TSH levels were higher than normal, TSH 20-70mIU/L, in spite of efforts to adjust the dose (different LT4 preparations). In last two years her daily LT4 dose was 900 (15 µg/kg), 3x300mcg, 500+400mcg. Comorbidities: depression, angina, hypertension, absolutely arrhythmias (with inadequate INR in last two months). Before testing TSH 33.6mIU/L, FT4 4.25 pmol/L. Standard (1000 µg) LAT was performed under supervision. TSH, T4 and FT4 were measured 2h, 4h, 6h and 24h upon LT4 administration. Baseline values were TSH 26.92 mIU/L; FT4 4.4pmol/L; T4 41.5pmol/L. The lack of TSH fall with slight T4 and FT4 increase, significantly below expected AUC, pointed an inadequate absorption. It was started with 300 µg LT4 oral suspension, after testing. The presence of fat in the stool and positive antiparietal antibodies increased suspicion to malabsorptiv syndrome. EGDS was performed, PH finding confirmed H. pylori positive chronic atrophic gastritis, without morphological elements for GSE. Eradication treatment and IPP were introduced. After four weeks her thyroid hormones were TSH 1.63 mIU/L; FT4 26.6pmol/L, FT3 3.87pmol/L. Conclusion: LAT is useful for identifying much rare malabsorption. The adequate treatment lead to proper substitution and avoidance of no rationale increase of levothyroxine dose.

Introduction: Adrenoleukodystrophy (ALD) is a disease characterized by the accumulation of very long chain fatty acids in tissues throughout the body. The most severely affected tissues are the myelin in the central nervous system, the adrenal cortex and the Leydig cells in the testes. Clinically, ALD is a heterogeneous disorder, presenting with several distinct phenotypes, and no clear pattern of genotype-phenotype correlation. Case report: Patients S.A. 50 years old, in the third year of life was diagnosed with primary adrenal insufficiency. From the age of 45 he feels, headache, dizziness, bends to the right when walking, night incontinence of urine. Talking to himself, the last year goes to the cemetery every day, occasionally crying without control and remembrance. Condition with spinocerebellar ataxia and a left pyramidal defect with incontinence of urine and psychiatric problems required re-examination. In consultation with neurologist at the Department of Neurology, investigations have shown that patient is suffering from X-linked adrenoleukodystrophy with affected central and peripheral nervous system. Adrenoleukodystrophy (ALD) is caused by mutations in ABCD1, a gene located on the X chromosome that codes for ALD, a peroxisomal membrane transporter protein. The exact mechanism of the pathogenesis of the various forms of ALD is not known. it is a disorder of peroxisomal fatty acid beta oxidation which results in the accumulation of very long chain fatty acids in tissues throughout the body. The most severely affected tissues are the myelin in the central nervous system, the adrenal cortex and the Leydig cells in the testes. Clinically, ALD is a heterogeneous disorder, presenting with several distinct phenotypes, and no clear pattern of genotype-phenotype correlation. As an X-linked disorder, ALD presents most commonly in males, however approximately 50% of heterozygote females show some symptoms later in life. Approximately two-thirds of ALD patients will present with the childhood cerebral form of the disease, which is the most severe form. It is characterized by normal development in early childhood, followed by rapid degeneration to a vegetative state. The other forms of ALD vary in terms of onset and clinical severity, ranging from adrenal insufficiency to progressive paraparesis in early adulthood (this form of the disease is typically known as adrenomyeloneuropathy). Conclusion: In our case hypocorticism was the first sign of X-linked adrenoleukodystrophy. In male patients with hypocorticism X-linked adrenoleukodystrophy should always be excluded as one of the possible causes of primary adrenal insufficiency.

OBJECTIVE: The aim of the study was to assess whether sudden change in blood glucose concentration in healthy subject would produce insulin secretory pattern similar to one in type 2 diabetic subjects (T2D). DESIGN: The concept of the study was to 'reset' the pancreas and empty the stored insulin pool, so that subtle derangements of the pulsatile insulin secretion could be studied. METHODS: The study group included 6 control and 7 T2D subjects. For insulin and glucose determination, blood was sampled for 60 minutes with 2 minutes inter-sample interval. To increase blood glucose an intravenous glucose bolus was given (0.3 g/kg body weight). RESULTS: The average glucose level in the T2D group was significantly higher, but the average insulin concentration was not different between the groups. Insulin half-life, pulse amplitude, number of pulses and interpulse interval did not differ between the groups. CONCLUSIONS: Therefore, the sudden increase in blood glucose causes insulin secretory pattern to become similar in the healthy and in the T2D subjects. However, the defect in the insulin secretion or glucose sensing inherent to β-cell exists, as the insufficient quantity of insulin is secreted in response to the increased glucose level.

Female pseudohermaphroditism represents discrepancy between karyotype and gonadal features on one side and a psychogenic phenotype on the other. Congenital adrenal hyperplasia is the part of the spectrum of female pseudohaermaofroditism and is due to an enzyme deficiency in steroidogenesis. More than 95% of patients have 21 hydroxylase deficiency which leads to a lack of cortisol and ACTH hypersecretion of pituitary, overproduction of 17 hydroxy progesterone (17OHP) and androgens and adrenal cortex hyperplasia. The clinical phenotype is classified as classical and nonclassical (aka. 'Late onset' form). The classic form is represented as salt-waisting and simply virilizing, depending on the degree of lack of aldosterone. Pathophysiology of CAH due to the lack of 21α hydroxylase is closely associated with the degree of enzyme deficiency. Overproduction of androgens is leading to accelerated virilisation. Classical form is manifested in childhood and is characterized by the overproduction of cortisol precursors and adrenal androgens. In the most severe form, co-aldosterone deficiency leads to loss of salt with all the complications. Girls with the classical form of CAH typically have am ambiguous genitals at birth due to high concentrations of androgens in utero. CAH due to 21OH deficiency is the most common cause of ambiguous genitals in 46XX newborns. Characteristically, the clitoris is enlarged, partially fused labia maiora and a common urogenital sinus at the site of the urethra and vagina. The uterus, Fallopian tubes and ovaries are present and normal, a structures of Wolfian duct are absent. When diagnosed in childhood 46XX CAH patients has been assigned female gender so far, even in fully expressed in virilised external genitalia. This dogmatic approach is based on preserving fertility, and if there was at least uterus, opting for female sex was considered justified. Only about 5% of 46 patients with XX KAH has a psychogenic male gender, as described patient. In addition to mutations of CYP21A2 and effects of high concentration of androgen in the CAH, in the phenotypic expression of CAH different length of sequence of CAG androgen receptor could have an impact, which modulates the effect of androgens on the periphery. Also, while the cases of adaptation of sexual identity and the external genitalia from female to male were documented, not a single case of questionable male sexual identity is noted. In the presented patient testosterone levels are at the upper limit for men, which may be due to enzymatic block and synthesis of cortisol precursor, which is further metabolized to the active androgen: testosterone and dihydrotestosterone. High concentrations of T prenatally and in infancy has led to premature fusion epiphysis and low growth, and high concentrations of DHT to clitoromegaly. The LHRH test showed no stimulatory response of LH, which is probably suppressed by high concentrations of testosterone , but there still needs to be done endocraniaol MNR to rule out other possible etiologies of gonadotroph suppression. Dexamethasone suppression test with measurement of testosterone could give an answer. The treatment of adult patients is based on hydrocortisone in dosages that provide permanent substitution of cortisol and suppress ACTH hypersecretion. In 46 XX patients who are phenotypically male, and whose full identity is male, reconstructive surgical procedures are needed to enable adequate quality of life.

Introduction. In interpreting thyroid hormones results it is preferable to think of interference and changes in concentration of their carrier proteins. Outline of Cases. We present two patients with discrepancy between the results of thyroid function tests and clinical status. The first case presents a 62-year-old patient with a nodular goiter and Hashimoto thyroiditis. Thyroid function test showed low thyroid-stimulating hormone (TSH) and normal to low fT4. By determining thyroid status (ТSH, T4, fT4, T3, fT3) in two laboratories, basal and after dilution, as well as thyroxine-binding globulin (TBG), it was concluded that the thyroid hormone levels were normal. The results were influenced by heterophile antibodies leading to a false lower TSH level and suspected secondary hypothyroidism. The second case, a 40-year-old patient, was examined and followed because of the variable size thyroid nodule and initially borderline elevated TSH, after which thyroid status showed low level of total thyroid hormones and normal TSH. Based on additional analysis it was concluded that low T4 and T3 were a result of low TBG. It is a hereditary genetic disorder with no clinical significance. Conclusion. Erroneous diagnosis of thyroid disorders and potentially harmful treatment could be avoided by proving the interference or TBG deficiency whenever there is a discrepancy between the thyroid function results and the clinical picture.

Among the many categories of images that require lossless compression, medical images can be indicated as one of the most important category. Medical image compression with loss impairs of diagnostic value, therefore, there are often legal restrictions on the image compression with losses. Among the common approaches to medical image compression we can distinguish the transformation-based and prediction-based approaches. This paper presents algorithms for the prediction based on the edge detection and estimation of local gradient. Also, a novel prediction algorithm based on advantages of standardized median predictor and gradient predictor is presented and analyzed. Removed redundancy estimation was done by comparing entropies of the medical image after prediction.

INTRODUCTION Endogenous Cushing's syndrome is a clinical state resulting from prolonged, inappropriate exposure to excessive endogenous secretion of Cortisol and hence excess circulating free cortisol, characterized by loss of the normal feedback mechanisms of the hypothalamo-pituitary-adrenal axis and the normal circadian rhythm of cortisol secretion [2]. The etiology of Cushing's syndrome may be excessive ACTH secretion from the pituitary gland, ectopic ACTH secretion by nonpituitary tumor, or excessive autonomous secretion of cortisol from a hyperfunctioning adrenal adenoma or carcinoma. Other than this broad ACTH-dependent and ACTH-independent categories, the syndrome may be caused by ectopic CRH secretion, PPNAD, MAH, ectopic action of GIP or catecholamines, and other adrenel-dependent processes associated with adrenocortical hyperfunction. CASE REPORT A 31 year-old men with b-month history of hyperpigmentation, weight gain and proximal myopathy was refereed to Institute of Endocrinology for evaluation of hypercortisolism. At admission, patient had classic cushingoid habit with plethoric face, dermal and muscle atrophy, abdominal strie rubrae and centripetal obesity. The standard laboratory data showed hyperglycaemia and hypokaliemia with high potassium excretion level. The circadian rhythm of cortisol secretion was blunted, with moderately elevated ACTH level, and without cortisol suppression after low-dose and high-dose dexamethason suppression test. Urinary 5HIAA was elevated. Abdominal and sellar region magnetic resonance imaging was negative. CRH stimulation resulted in ACTH increase of 87% of basal, but without significant increase of cortisol level, only 7%. Thoracal CT scan revealed 14 mm mass in right apical pulmonary segment. A wedge resection of anterior segment of right upper lobe was performed. Microscopic evaluation showed tumor tissue consisting of solid areas of uniform, oval cells with eosinophilic cytoplasm and centrally located nuclei. Stromal tissue was scanty, and mitotic figures were infrequent. Tumor cells were immunoreactive for synaptophysin, neuron-specific enolase, and ACTH. The postoperative course was uneventful and the patient was discharged on glucocorticoid supplementation. Signs of Cushing's syndrome were in regression, and patient remained normotensive and normoglycaemic without therapy. DISCUSSION A multitude of normal nonpituitary cells from different organs and tissues have been shown to express the POMC gene from which ACTH is derived. The tumors most commonly associated the ectopic ACTH syndrome arise from neuroendocrine tissues, APUD cells. POMC gene expression in non-pituitary cells differs from that in pituitary cells both qualitatively and quantitatively [8], Aggressive tumors, like small cell cancer of the lung (SCCL) preferentially release intact POMC, whereas carcinoids rather overprocess the precursor, releasing ACTH and smaller peptides like CLIP. Some tumors associated with ectopic ACTH syndrome express other markers of neuroendocrine differentiation like two specific prohormone convertases (PCs). Assessment of vasopressin (V3) receptor gene expression in ACTH-producing nonpituitary tumors revealed bronchial carcinoid as a particular subset of tumors where both V3 receptor and POMC gene may be expressed in pattern indistinguishable from that in corticotroph adenoma [9]. In most, but not all, patients with ectopic ACTH syndrome, cortisol is unresponsive to high-dose dexamethason suppression test, what is used as diagnostic tool. It is not clear if the primary resistance resulted from structural abnormality of the native glucocorticoid receptor (GR), a low level of expression, or some intrinsic property of the cell line [9]. It appears that ectopic ACTH syndrome is made of two different entities. When it is because of highly differentiated tumors, with highest level of pituitary-like POMC mRNA, expressing PCs, high level of V3 receptors and GR, like bronchial carcinoids, it might be called ectopic corticotroph syndrome. In contrast, when it is caused by aggressive, poorly differentiated tumors, with much lower expression of V3 receptor, like SCCL, it might be called aberrant ACTH secretion syndrome. Carcinoid tumors have been reported in a wide range of organs but most commonly involve the lungs, bronchi, and gastrointestinal tract. They arise from neuroendocrine cells and are characterized by positive reactions to markers of neuroendocrine tissue, including neuron specific enolase, synaptophysin, and chromogranina [11]. Carcinoid tumors are typically found to contain numerous membrane-bound neurosecretory granules composed of variety of hormones and biogenic amines. One of the best characterized is serotonin, subsequently metabolized to 5-hydrohy-indolacetic acid (5-HIAA), which is excreted in the urine. In addition to serotonin, carcinoid tumors have been found to secrete ACTH, histamine, dopamine, substance P, neurotensin, prostaglandins and kallikrein. The release of serotonin and other vasoactive substances is thought to cause carcinoid syndrome, which manifestations are episodic flushing, weezing, diarrhea, and eventual right-sided valvular heart disease. These tumors have been classified as either well-differentiated or poorly differentiated neuroendocrine carcinomas. The term „pulmonary tumorlets" describes multiple microscopic nests of neuroendocrine cells in the lungs [12]. Pulmonary carcinoids make up approximately 2 percents of primary lung tumors. The majority of these tumors are perihilar in location, and patients often presents with recurrent pneumonia, cough, hemoptisis, or chest pain. The carcinoid syndrome occurs in less than 5 percent of cases. Ectopic secretion of ACTH from pulmonary carcinoid accounts for 1 percent of all cases of Cushing's syndrome. They are distinct clinical and pathologic entity, generally peripheral in location. Although they are usually typical by standard histologie criteria, they have mush greater metastatic potential than hormonally quiescent typical carcinoids [13]. Surgical treatment therefore should be one proposed for more aggressive malignant tumors. In all cases of ACTH-dependent Cushing's syndrome with regular pituitary MRI and bilateral inferior petrosal sinus sampling, thin-section and spiral CT scanning of the chest should be routine diagnostic procedure [14], We present thirty-one year old patient with typical pulmonary carcinod with ACTH ectopic secretion consequently confirmed by histology.

Chronic fatigue syndrome (CFS) is defined as constellation of the prolonged fatigue and several somatic symptoms, in the absence of organic or severe psychiatric disease. However, this is an operational definition and conclusive biomedical explanation remains elusive. Similarities between the signs and symptoms of CFS and adrenal insufficiency prompted the research of the hypothalamo-pituitary-adrenal axis (HPA) derangement in the pathogenesis of the CFS. Early studies showed mild glucocorticoid deficiency, probably of central origin that was compensated by enhanced adrenal sensitivity to ACTH. Further studies showed reduced ACTH response to vasopressin infusion. The response to CRH was either blunted or unchanged. Cortisol response to insulin induced hypoglycaemia was same as in the control subjects while ACTH response was reported to be same or enhanced. However, results of direct stimulation of the adrenal cortex using ACTH were conflicting. Cortisol and DHEA responses were found to be the same or reduced compared to control subjects. Scott et all found that maximal cortisol increment from baseline is significantly lower in CFS subjects. The same group also found small adrenal glands in some CFS subjects. These varied and inconsistent results could be explained by the heterogeneous study population due to multifactorial causes of the disease and by methodological differences. The aim of our study was to assess cortisol response to low dose (1 µg) ACTH using previously validated methodology. We compared cortisol response in the CFS subjects with the response in control and in subjects with suppressed HPA axis due to prolonged corticosteroid use. Cortisol responses were analyzed in three subject groups: control (C) secondary adrenal insufficiency (AI), and in CFS. The C group consisted of 39 subjects, AI group of 22, and CFS group of nine subjects. Subject data are presented in table 1. Low dose ACTH test was started at 0800 h with the iv injection of 1 µg ACTH (Galenika, Belgrade, Serbia). Blood samples for cortisol determination were taken from the iv cannula at 0,15, 30, and 60 min. Data are presented as mean standard error (SE). Statistical analysis was done using ANOVA with the Games-Howell post-hoc test to determine group differences. ACTH dose per kg or per square meter of body surface was not different between the groups. Baseline cortisol was not different between the groups. However, cortisol concentrations after 15 and 30 minutes were significantly higher in the C group than in the AI group. Cortisol concentration in the CFS group was not significantly different from any other group (Graph 1). Cortisol increment at 15 and 30 minutes from basal value was significantly higher in C group than in other two groups. However there was no significant difference in cortisol increment between the AI and CFS groups at any time of the test. On the contrary, maximal cortisol increment was not different between CFS and other two groups, although it was significantly higher in C group than in the AI group. Maximal cortisol response to the ACTH stimulation and area under the cortisol response curve was significantly larger in C group compared to AI group, but there was no difference between CFS and other two groups. Several previous studies assessed cortisol response to ACTH stimulation. Hudson and Cleare analysed cortisol response to 1 µg ACTH in CFS and control subjects.They compared maximum cortisol attained during the test, maximum cortisol increment, and area under the cortisol response curve.There was no difference between the groups in any of the analysed parameters. However, authors commented that responses were generally low. On the contrary Scott et all found that cortisol increment at 30 min is significantly lower in the CFS than in the control group. Taking into account our data it seems that the differences found in previous studies papers are caused by the methodological differences. We have shown that cortisol increment at 15 and 30 min is significantly lower in CFS group than in C group. Nevertheless, maximum cortisol attained during the test, maximum cortisol increment, and area under the cortisol response curve were not different between the C and CFS groups. This is in agreement with our previous findings that cortisol increment at 15 minutes has the best diagnostic value of all parameters obtained during of low dose ACTH test. However, there was no difference between CFS and AI group in any of the parameters, although AI group had significantly lower cortisol concentrations at 15 and 30 minutes, maximal cortisol response, area under the cortisol curve, maximal cortisol increment, and maximal cortisol change velocity than C group. Consequently reduced adrenal responsiveness to ACTH exists in CFS. In conclusion, we find that regarding the adrenal response to ACTH stimulation CFS subjects present heterogeneous group. In some subjects cortisol response is preserved, while in the others it is similar to one found in secondary adrenal insufficiency.

Developing highly efficient semiconductor metal oxide (SMOX) sensors capable of accurate and fast responses to environmental humidity is still a challenging task. In addition to a not so pronounced sensitivity to relative humidity change, most of the SMOXs cannot meet the criteria of real-time humidity sensing due to their long response/recovery time. The way to tackle this problem is to control adsorption/desorption processes, i.e., water-vapor molecular dynamics, over the sensor's active layer through the powder and pore morphology design. With this in mind, a KIT-5-mediated synthesis was used to achieve mesoporous tin (IV) oxide replica (SnO2-R) with controlled pore size and ordering through template inversion and compared with a sol-gel synthesized powder (SnO2-SG). Unlike SnO2-SG, SnO2-R possessed a high specific surface area and quite an open pore structure, similar to the KIT-5, as observed by TEM, BET and SWAXS analyses. According to TEM, SnO2-R consisted of fine-grained globular particles and some percent of exaggerated, grown twinned crystals. The distinctive morphology of the SnO2-R-based sensor, with its specific pore structure and an increased number of oxygen-related defects associated with the powder preparation process and detected at the sensor surface by XPS analysis, contributed to excellent humidity sensing performances at room temperature, comprised of a low hysteresis error (3.7%), sensitivity of 406.8 kΩ/RH% and swift response/recovery speed (4 s/6 s). [ABSTRACT FROM AUTHOR]

In the present work, a biomaterial (SBA‐16/HA) based on the growth of hydroxyapatite (HA) particles within an organized silica structure SBA‐16 (Santa Barbara Amorphous‐16) was developed to evaluate its application to act as a porous microenvironment promoting attachment and viability of human dental pulp stem cells of healthy deciduous teeth (SHED). First, SHED were isolated and their phenotypes were evaluated by flow cytometry. The samples of SBA‐16/HA were characterized by X‐ray diffraction (XRD), small and wide angle X‐ray scattering (SWAXS), Fourier transform infrared spectroscopy (FTIR), and scanning electron microscopy (SEM) equipped with energy dispersive spectra detector (EDS). Afterward, cells were cultured in the eluates of the above‐mentioned biomaterial aged for 24 hr, 7. and 14 days. Bio‐Oss® and dentin particles are involved for comparison and cells are cultured in the eluates of these two materials also. Thiazolyl Blue Tetrazolium bromide assay‐MTT (3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐Diphenyltetrazolium Bromide assay) was used for the determination of cell viability. The results obtained by all aforementioned characterization methods of SBA‐16/HA, revealed a uniform spherical mesoporous structure, an intrinsic characteristic of this material. This material displayed excellent biocompatibility on SHEDs, and even proliferative potential, indicating that SBA‐16/HA could potentially serve as a suitable substrate for bone regeneration. Contrary to SBA‐16/HA, dentin particles showed low cytotoxicity at all time points, compared to control and Bio‐Oss®groups. Our results substantiate the idea that SBA‐16/HA has a beneficial effect on SHEDs, thus paving the way toward developing new material for bone replacement. [ABSTRACT FROM AUTHOR]